Abstract
AbstractCentral glucose availability is a critical monitored variable in the regulation of reproductive neuroendocrine function. While current studies implicate the periventricular caudal brainstem as a source of signaling of decreased availability of catabolic intermediates and/or glycolytic end products, the mechanisms by which local metabolic ‘sensors’ signal diminished glucose utilization are not clear. The present experiments investigated whether fourth ventricular infusion of the aerobic catabolic substrate, lactate, attenuates glucoprivic suppression of luteinizing hormone (LH). Cyclic female rats were injected at 13.00h on proestrus with the glucose antimetabolite, 2‐deoxy‐D‐glucose (2DG; 50 vs. 150ug), or vehicle into the rostral fourth ventricle. Additional proestrus animals were treated by continuous fourth ventricular infusion of 10.0 µM lactate/hr or vehicle, initiated prior to ip injection of 400mg 2DG/kg bw or saline. Serial blood samples were obtained hourly during proestrus afternoon for radioimmunoassay of plasma LH. The results demonstrate a reduction in the LH surge following icv 2DG administration, while showing that fourth ventricular infusion of lactate reversed inhibition of hormone release by systemic antimetabolite administration. These findings support the view that hindbrain signaling of glucose metabolic dysfunction initiates neural mechanisms that inhibit the proestrus LH surge, and that lactate utilization may be monitored as an indicator of local cellular energy stasis.
Published Version
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